A patient who stops taking an ACE inhibitor because of its side effects will begin taking an angiotensin II receptor blocker (ARB) medication. Which side effect of ACE inhibitors will not occur with an ARB medication?

Choice A reason: Morphine, an opioid, binds to mu, kappa, and delta receptors in the brain, spinal cord, and gastrointestinal tract. Mu receptors in the gut slow peristalsis, causing constipation, while central receptors relieve pain. This multi-receptor binding explains both therapeutic and side effects, making this the correct choice.

Choice B reason: Constipation from morphine occurs at therapeutic, not just toxic, doses due to mu receptor activation in the gastrointestinal tract, which reduces motility. Toxicity may worsen side effects, but constipation is a common effect at standard doses, making this choice inaccurate for explaining morphine’s mechanism.

Choice C reason: Morphine’s receptors (e.g., mu) regulate multiple processes, but the drug itself isn’t selective to multifunctional receptors. It binds broadly to opioid receptors, causing both analgesia and side effects like constipation. This choice misrepresents morphine’s non-selective binding, making it less accurate than choice A.

Choice D reason: Morphine’s effects, including analgesia and constipation, result from specific receptor binding, not coincidental processes. It activates opioid receptors in the brain for pain relief and in the gut for reduced motility. This choice incorrectly suggests constipation is unrelated to morphine’s pharmacological action, making it incorrect.

Choice A reason: Decreased blood pressure triggers the baroreceptor reflex, increasing sympathetic activity to raise heart rate and vasoconstriction to restore pressure. A decreased heart rate would occur with increased blood pressure, not hypotension, as parasympathetic activation dominates. This choice is incorrect as it opposes the body’s compensatory response to low blood pressure.

Choice B reason: Erythema, or skin redness, results from vasodilation or inflammation, not directly from hypotension. While compensatory vasoconstriction occurs in hypotension, it reduces skin perfusion, potentially causing pallor, not erythema. This manifestation is unrelated to the cardiovascular response to decreased blood pressure, making this choice incorrect.

Choice C reason: Increased temperature is not a direct response to decreased blood pressure. Hypotension triggers sympathetic activation, prioritizing heart rate and vasoconstriction to maintain perfusion. Temperature changes may occur in shock states, but they’re not primary manifestations of routine hypotension, making this choice irrelevant to the expected clinical response.

Choice D reason: Decreased blood pressure activates the baroreceptor reflex, stimulating sympathetic nervous system activity. This increases heart rate (tachycardia) to enhance cardiac output, compensating for low pressure to maintain tissue perfusion. This is a primary physiological response to hypotension, making it the correct clinical manifestation expected in this scenario.